Denise Traxler1, Matthias Zimmermann2, Elisabeth Simader3, Cecilia M Veraar4, Bernhard Moser5, Thomas Mueller6, Michael Mildner7, Varius Dannenberg8, Mitja Lainscak9, Borut Jug10, Hendrik J Ankersmit11. 1. Division of Cardiology, Department of Internal Medicine II, Medical University of Vienna, Waehringer Guertel 18-20, 1090 Vienna, Austria; Laboratory for Cardiac and Thoracic Diagnosis, Regeneration and Applied Immunology, Waehringergürtel 18-20, 1090 Vienna, Austria; Division of Thoracic Surgery, Department of Surgery, Medical University of Vienna, Waehringer Guertel 18-20, 1090 Vienna, Austria. 2. Department of Oral and Maxillofacial Surgery, Medical University of Vienna, Waehringer Guertel 18-20, 1090 Vienna, Austria. 3. Laboratory for Cardiac and Thoracic Diagnosis, Regeneration and Applied Immunology, Waehringergürtel 18-20, 1090 Vienna, Austria; Division of Thoracic Surgery, Department of Surgery, Medical University of Vienna, Waehringer Guertel 18-20, 1090 Vienna, Austria; Division of Rheumatology, Department of Internal Medicine III, Medical University of Vienna, Waehringer Guertel 18-20, 1090 Vienna, Austria. 4. Division of Cardiothoracic and Vascular Anaesthesia and Intensive Care Medicine, Department of Anaesthesia, Intensive Care Medicine, and Pain Medicine, Medical University of Vienna, Waehringer Guertel 18-20, 1090, Vienna, Austria. 5. Division of Thoracic Surgery, Department of Surgery, Medical University of Vienna, Waehringer Guertel 18-20, 1090 Vienna, Austria. 6. Department of Clinical Pathology, Hospital of Bolzano, Lorenz Böhler Straße 5, 39100 Bolzano, Italy. 7. Research Division of Biology and Pathobiology of the Skin, Department of Dermatology, Medical University of Vienna, Waehringer Guertel 18-20, 1090 Vienna, Austria. 8. Division of Cardiology, Department of Internal Medicine II, Medical University of Vienna, Waehringer Guertel 18-20, 1090 Vienna, Austria. 9. Division of Cardiology, General Hospital Murska Sobota, Ulica dr. Vrbnjaka 6, 9000 Murska Sobota, Slovenia; Faculty of Medicine, University of Ljubljana, Korytkova ulica 2, 1000 Ljubljana, Slovenia. 10. Department of Vascular Diseases, Division of Internal Medicine, University Clinical Center, Zaloška 7/VI, SI-1000 Ljubljana, Slovenia. 11. Division of Thoracic Surgery, Department of Surgery, Medical University of Vienna, Waehringer Guertel 18-20, 1090 Vienna, Austria. Electronic address: hendrik.ankersmit@meduniwien.ac.at.
Abstract
BACKGROUND: The inflammatory markers sST2, HSP27 and hsCRP have already been identified as prognostic markers in chronic heart failure (HF). Though individual biomarkers have proven their value in mortality risk prediction, the role of a multimarker strategy needs further evaluation. MATERIALS AND METHODS: This is an exploratory reanalysis in chronic HF patients. Plasma HSP27, sST2 and hsCRP in outpatients with chronic HF were analysed. Patients were followed for a minimum of twelve months for the endpoint cardiovascular mortality and unplanned HF associated hospitalisation (=event). 15 year overall mortality was assessed retrospectively. The prognostic impact was assessed using a Cox proportional hazard model. RESULTS: 113 chronic HF patients were included. Median follow up time was 614 days and 37 patients (32.7%) experienced an event. A Kaplan-Meier analysis revealed that patients with increased sST2, HSP27 and hsCRP levels have significantly worse prognosis (p < 0.001). The use of a three-biomarker combination was superior in an independent risk prediction of an event (one high vs. two high: HR = 4.5, 95% CI: 1.3-15.5, p = 0.018; and one high vs. all high: HR = 9.8, 95% CI: 2.8-34.3, p < 0.001) as shown in a multivariable cox proportional hazard model. However, the biomarker panel did not predict 15 year overall mortality, in contrast to elevated HSP27 levels (p = 0.012). CONCLUSIONS: The combination of all three markers is an independent predictor of cardiovascular death and unplanned HF associated hospitalisation but not overall mortality. Our findings suggest that adding those markers in combination to well established risk assessment parameters may improve risk stratification.
BACKGROUND: The inflammatory markers sST2, HSP27 and hsCRP have already been identified as prognostic markers in chronic heart failure (HF). Though individual biomarkers have proven their value in mortality risk prediction, the role of a multimarker strategy needs further evaluation. MATERIALS AND METHODS: This is an exploratory reanalysis in chronic HF patients. Plasma HSP27, sST2 and hsCRP in outpatients with chronic HF were analysed. Patients were followed for a minimum of twelve months for the endpoint cardiovascular mortality and unplanned HF associated hospitalisation (=event). 15 year overall mortality was assessed retrospectively. The prognostic impact was assessed using a Cox proportional hazard model. RESULTS: 113 chronic HF patients were included. Median follow up time was 614 days and 37 patients (32.7%) experienced an event. A Kaplan-Meier analysis revealed that patients with increased sST2, HSP27 and hsCRP levels have significantly worse prognosis (p < 0.001). The use of a three-biomarker combination was superior in an independent risk prediction of an event (one high vs. two high: HR = 4.5, 95% CI: 1.3-15.5, p = 0.018; and one high vs. all high: HR = 9.8, 95% CI: 2.8-34.3, p < 0.001) as shown in a multivariable cox proportional hazard model. However, the biomarker panel did not predict 15 year overall mortality, in contrast to elevated HSP27 levels (p = 0.012). CONCLUSIONS: The combination of all three markers is an independent predictor of cardiovascular death and unplanned HF associated hospitalisation but not overall mortality. Our findings suggest that adding those markers in combination to well established risk assessment parameters may improve risk stratification.